PDGFRA (Platelet Derived Growth Factor Receptor Alpha)

Neonatal PDGFRα+ cells proliferated and differentiated into MBP- and QKI7-positive oligodendrocytes. This approach provides a practical platform for studying oligodendrocyte biology and evaluating therapeutic vectors and other interventions in myelin disorders.

Integrated clinicopathologic and molecular assessment reclassified most HEPU cases as reactive or clonal, with only 39% remaining idiopathic. Myeloid NGS frequently identifies clonal variants critical for refining HE classification, although results require cautious interpretation within the WHO-HAEM5 and ICC 2022 context.

These findings highlight the anticancer potential of P. acutifolia EOs as candidates for future pharmaceutical examination.

This case represents the first documented instance of primary gliosarcoma with FDCS differentiation, thereby expanding its known differentiation spectrum. Furthermore, it demonstrates the necessity of separately analyzing each histological component in the diagnosis of challenging cases.

These findings provide the first comprehensive characterization of germline and somatic alterations in Tunisian TNBC patients, representing a North African cohort. They reveal the heterogeneity of mutation patterns linked to treatment response, and emphasize the importance of genomic profiling into clinical practice and guide personalized therapeutic strategies.

Small intestinal GISTs are relatively uncommon, and epithelioid-type GISTs that are KIT-negative and DOG1-negative are extremely rare. This case highlights the importance of considering atypical GISTs in the differential diagnosis of small bowel tumors with unusual immunohistochemical features.

P1, N=278, Recruiting, IDRX, Inc., a wholly owned subsidiary of GSK, LLC | Trial completion date: Nov 2027 --> Jun 2028 | Trial primary completion date: Nov 2027 --> Mar 2027

Activating mutations in KIT or PDGFRA characterize most GISTs and confer sensitivity to imatinib, whereas succinate dehydrogenase (SDH)–deficient GISTs lack these mutations and are typically imatinib resistant...Pathology demonstrated spindle cell GIST with significant treatment effect and retained SDHB expression. This case suggests that oncogenic KIT signaling may remain the dominant driver of GIST behavior despite the presence of a germline SDHC mutation and highlights the importance of integrated molecular interpretation in GIST management.

Although tyrosine kinase inhibitors (TKIs), particularly imatinib, have substantially improved outcomes, most patients with advanced disease eventually develop resistance, resulting in disease progression...Molecular stratification and personalized approaches dominate ongoing research, but evidence generation remains limited by small sample sizes and slow recruitment. Future trials integrating innovative therapeutic platforms and patient-centered outcomes are essential to improve long-term disease control and quality of life.

Kaplan-Meier analysis on 1336 CRC patients indicated that high expression of CITED2, CPE, and Ang2 is associated with reduced overall survival. Collectively, these findings suggest that TEM infiltration is linked to transcriptional regulation, biological processes, and enzymatic programs in CRC, potentially contributing to tumor progression and poor prognosis, and highlight CCR7, PDGFRA, CITED2, CPE, and Ang1 as candidate biomarkers for further mechanistic exploration.

Compound juvenile Pdgfrα-CreER;Ext1f/f and Fgf18-CreER;Ext1f/f mice were injected with tamoxifen and monitored for tumor development over time...Analyses also showed that the developing osteochondromas in the Pdgfrα;Ext1 mutants displayed strong expression of cartilage proteins and abundant pSMAD1 and pSMAD2 proteins that mediate pro-chondrogenic BMP/TGFβ signals. The data provide new evidence that perichondrium progenitors, and more specifically inner layer cells delineated by Pdgfrα expression, initiate osteochondroma formation, being redirected into an ectopic chondrogenic program by Ext1 loss and deficiency of its vital function.

Clinically, elevated TRIM21 expression correlated with poor patient survival and confers resistance to both conventional radio-chemotherapy and the PDGFRA-targeted tyrosine kinase inhibitor imatinib in PDGFRA-high GBM. Our integrated analysis revealed an inverse correlation between TRIM21 and PDGFRA protein levels in patient specimens and highlighted TRIM21 upregulation as a feature of advanced disease. Collectively, these findings unveiled a crucial regulatory axis wherein TRIM21 switched PDGFRA from a context-dependent protective factor to an oncogenic driver and revealed TRIM21 as a prognostic biomarker and a therapeutic target for the PDGFRA-amplified subset of GBM.